Tríada találgica. Una nueva entidad clínica a partir de una serie de casos / Thalalgic triad. A new clinical entity from a case series

Introducción: El dolor crónico en el talón es un cuadro frecuente en la patología del pie. Este tipo de cuadros no están causados por una sola lesión, sino que es el resultado de la combinación de una serie de cuadros clínicos, especialmente por una neuropatía de Baxter y una fascitis plantar. Desde hace varios años, y tras analizar una serie de casos clínicos, se observa que los pacientes con dolor crónico en el talón cursan con un proceso de fasciosis plantar, edema óseo de calcáneo o síndrome congestivo de calcáneo y neuropatía del nervio de Baxter. A raíz de este hallazgo concluimos en una nueva entidad clínica denominada tríada találgica, la cual no presenta referencias bibliográficas anteriores en la literatura científica. Pacientes y métodos: Se ha llevado a cabo una serie de casos de 10 pacientes a los que se les diagnostica una combinación de 3 patologías, denominada tríada találgica, que cursa con aparición de fasciosis plantar, edema óseo de calcáneo (congestión calcánea) y neuropatía compresiva de Baxter. Cada una de estas patologías se trata de forma independiente con distintas terapias, tales como soportes plantares, infiltraciones, tratamiento farmacológico o cirugía. Resultados: Un total de 10 mujeres con una edad media de 53 años fueron diagnosticadas de fasciosis plantar, edema óseo de calcáneo y neuropatía compresiva de Baxter mediante diferentes pruebas, como la ecografía. Estas pacientes fueron tratadas mediante infiltraciones de colágeno, extracción del líquido sanguinolento del calcáneo, terapia electrolisis percutánea intratisular, soportes plantares, tratamiento farmacológico y ondas de choque. El 40 % de la muestra se encontraba de baja laboral debido al dolor incapacitante de esta tríada y el 10 % en situación de jubilación. Conclusiones: La tríada találgica es una entidad clínica desconocida, con un diagnóstico complejo que combina pruebas complementarias con diagnóstico clínico...(AU)

Introduction: Chronic heel pain is a frequent condition in foot pathology. These types of pictures are not caused by a single injury, but are the result of a combination of a series of clinical pictures, especially Baxter's neuropathy and plantar fasciitis. For several years and after analyzing a series of clinical cases, it has been observed that patients with chronic pain in the heel present with a process of plantar fasciosis, calcaneal bone edema or congestive calcaneal syndrome and Baxter nerve neuropathy. As a result of this finding, we conclude on a new clinical entity called thatalgic triad, which does not present previous bibliographic references in the scientific literature. Patients and methods: A series of cases of 10 patients who were diagnosed with a combination of 3 pathologies, called the thatalgic triad, has been carried out, with the appearance of plantar fasciosis, calcaneal bone edema (calcaneal congestion) and neuropathy Baxter compression. Each of these pathologies is treated independently with different therapies, such as plantar supports, infiltrations, drug treatment or surgery. Results: A total of 10 women with a mean age of 53 years were diagnosed with plantar fasciosis, calcaneal bone edema and Baxter's compressive neuropathy by different tests, such as ultrasound. These patients were treated by collagen infiltrations, removal of bloody fluid from the calcaneus, intratissular percutaneous electrolysis therapy, plantar supports, pharmacological treatment, and shock waves. 40 % of the sample was on sick leave due to the disabling pain of this triad and 10 % were in retirement. Conclusions: The thatalgic triad is an unknown clinical entity with a complex diagnosis that combines complementary tests with clinical diagnosis. Likewise, there are very few bibliographic references on this subject.(AU)

The differential response of astrocytes within the vestibular and cochlear nuclei following unilateral labyrinthectomy or vestibular afferent activity blockade by transtympanic tetrodotoxin injection in the rat.

In this study, we investigated whether changes in the vestibular neuronal activity per se influence the pattern of astrocytes morphology, glial fibrillary acidic protein (GFAP) expression and ultimately their activation within the vestibular nuclei after unilateral transtympanic tetrodotoxin (TTX) injections and after unilateral inner ear lesion. The rationale was that, theoretically the noninvasive pharmacological functional blockade of peripheral vestibular inputs with TTX, allowed us to dissociate the signals exclusively related to the shutdown of the resting activity of the first-order vestibular neurons and from neuronal signals associated with trans-ganglionic changes in first order vestibular neurons induced by unilateral labyrinthectomy (UL). Since the cochlea was removed during the surgical procedure, we also studied the astrocytic reaction within the deafferented cochlear nuclei. No significant changes in the distribution or relative levels of GFAP mRNA expression, relative levels of GFAP protein or immunoreactivity for GFAP were found in the ipsilateral vestibular nuclei at any post-TTX injection times studied. In addition, no sign of microglia activation was observed. In contrast, a robust increase of the distribution and relative levels of GFAP mRNA expression, protein levels and immunoreactivity was observed in the deafferented vestibular and cochlear nuclei beginning at 1 day after inner ear lesion. GFAP mRNA expression and immunoreactivity in the cochlear nucleus was qualitatively stronger than in the ipsilateral vestibular nuclei. The results suggest that astrocyte activation in the vestibular nuclei is not related to drastic changes of vestibular nuclei neuronal activity per se. Early trans-ganglionic changes due to vestibular nerve dendrites lesion provoked by the mechanical destruction of vestibular receptors, most probably induced the glial reaction. Its functional role in the vestibular compensation process remains to be elucidated.

Cochlear electrical stimulation: influence of age of implantation on Fos immunocytochemical reactions in inferior colliculi and dorsal cochlear nuclei of the rat.

The influence of age at the time of implantation of a stimulating electrode unilaterally in the inner ear on central auditory pathways was investigated in rats deafened shortly after birth. Immunoreactivity for Fos served as a functional marker of neuronal activity. Electrodes were implanted in the left cochlea of rats aged 3 weeks or 4 months. Stimulation lasted 45 minutes, then rats were sacrificed and tissues processed for immunocytochemistry. The younger animals showed significantly more neurons with Fos immunoreactivity bilaterally in the dorsal cochlear nuclei (DCN) and inferior colliculi (IC) than the older rats or control animals with normal hearing receiving the same stimulation. Activity was more prominent in the left DCN and right IC. The results show that electrical stimulation of the inner ear is more effective in younger animals in eliciting gene expression associated with development of a functional network in the auditory pathways. This suggests that deaf children should be provided with cochlear implants as early as possible.

Lack of growth-associated protein-43 reemergence or of growth-associated protein-43 mRNA modulation in deafferented vestibular nuclei during the first 6 weeks after unilateral inner ear lesion.

We investigated whether a unilateral inner ear lesion that destroyed the labyrinthine receptors, the cochlear receptors, and the spiral ganglion induced collateral sprouting in rat vestibular and auditory brainstem nuclei, using growth-associated protein-43 (GAP-43) as an indicator of synaptic remodeling. Both immunocytochemistry and in situ hybridization were performed to detect a potential modulation of GAP-43 and of its messenger RNA (mRNA) at different times after surgery. We failed to observe a reemergence of GAP-43 or a modulation of its mRNA in the deafferented vestibular nuclei at all survival times tested. In contrast, a substantial increase in the expression of GAP-43 was observed in the neuropil of the ipsilateral deafferented cochlear nuclei and in cell bodies of the ipsilateral superior olive. This increase was associated with an up- and downregulation of the mRNA coding for GAP-43 in the ipsilateral ventral cochlear nucleus and in the ipsilateral superior olive, respectively. These data indicate that synaptic remodeling, as assessed by GAP-43 expression, does not seem to occur in the deafferented vestibular complex during the first 6 weeks after labyrinthectomy, whereas it occurs within the first deafferented auditory relays at times as early as 4 days following spiral ganglion and cochlear receptors removal. We conclude that recovery of a normal resting discharge of the deafferented central vestibular neurons and consequently recovery of a normal resting posture and eye position may not depend on collateral sprouting of the remaining vestibular afferents. In contrast, we confirmed that a reactive synaptogenesis occurs in the brainstem auditory nuclei following cochlea and spiral ganglion removal. Its functional significance remains an open question.

Evidence for a microglial reaction within the vestibular and cochlear nuclei following inner ear lesion in the rat.

Following unilateral inner ear lesion, astrocytes undergo hypertrophy in the deafferented vestibular and cochlear nuclei as shown by an increase in the level of glial fibrillary acid. The present study extends our understanding of vestibular and cochlear system plasticity by examining microglial changes in these deafferented nuclei. The microglial reaction was studied 1, 2, 4, 8, 14, 21, 28 and 42 days following the lesion with a monoclonal OX-42 antibody and lectins (Griffonia simplicifolia, B4 isolectin) labelled with horseradish peroxidase or fluorescein. The deafferented nuclei were also examined for apoptotic cells by terminal transferase-mediated nick end labelling of nuclear DNA fragments. In control and sham-operated rats, the distribution of the resting microglial cells was uniform in both the vestibular and cochlear nuclei. In the deafferented vestibular complex, the microglial cells increased in number, became hypertrophied and were distributed in the medial, lateral, superior and inferior vestibular nuclei. Reactive microglial cells were also detected in the ipsilateral cochlear nuclei. Some of the immunostained cells were hypertrophic whereas others presented an ameboid morphology with few short and stout processes. The microglial reaction was confined to the antero- and posteroventral cochlear nuclei. Finally, reactive microglia was also observed in the prepositus hypoglossi ipsilateral to the lesion. The microglial reactions within the prepositus hypoglossi, the vestibular and the cochlear nuclei were detectable as early as one day after the lesion and persisted several weeks in both the vestibular and cochlear nuclei. Apoptotic cells were not detected in the vestibular nuclei at any stage following the lesion. In contrast, terminal deoxynucleotidyl transferase-mediated digoxygenin-11-dUTP nick end labelling-positive cells were first detected in the deafferented cochlear nuclei on the 3rd day following the lesion. They reached an apparent maximum by day 8 and then declined until day 24. Double labelling experiments demonstrate that these cochlear terminal deoxynucleotidyl transferase-mediated digoxygenin-11-dUTP nick end labelling-positive cells were also lectin-positive suggesting that reactive cochlear lectin-positive microglia cells were eliminated by a programmed cell death. Our results establish the two experimental models as reliable tools to understand the role of microglia in adult brain plasticity. The cochlear microglial reaction was probably induced by the degeneration of the acoustic nerve which follows the acoustic ganglion destruction. Interestingly, the same reasoning cannot apply to the vestibular microglial reaction following unilateral labyrinthectomy: the vestibular ganglion was spared and the primary vestibular neurons did not degenerate, at least during the first week following the lesion.

Evidence for reactive astrocytes in rat vestibular and cochlear nuclei following unilateral inner ear lesion.

We investigated whether unilateral removal of the labyrinthine and cochlear receptors induces a macroglial reaction in rat vestibular and cochlear nuclei using vimentin and glial fibrillary acidic protein (GFAP) immunochemical markers. Antibody binding was visualized using the avidin-biotin method and 3,3'-diaminobenzidine as the peroxidase substrate. In addition, double-labelling experiments were performed using specific secondary fluorescent antibodies. Potentially degenerating axon terminals were also studied using a silver impregnation method. In normal adult rats, vimentin was found only in ependymal cells, tanicytes around the fourth ventricle, endothelial cells in the blood vessels and Bergmann glia in the molecular layer of the cerebellum. In lesioned rats, all deafferented vestibular and ventral cochlear nuclei showed strong vimentin immunoreactivity. Furthermore, double-labelling experiments demonstrated that these vimentin-positive cells were also GFAP-positive. The reaction became evident on the second day after the lesion, was intense for 3-8 days and then declined until day 21. No vimentin immunoreactivity could be detected at the level of the ipsilateral dorsal cochlear nucleus. Therefore, unilateral inner ear lesion induced an astroglial reaction within the deafferented vestibular and cochlear nuclei. The decrease in the resting discharge of the primary vestibular afferents and/or in the deafferented central vestibular neurons may induce the glial reaction in the vestibular complex, whereas both degeneration and silence of the cochlear nerve and central cochlear neurons are most probably responsible for the cochlear vimentin-immunoreactive staining. The role of the reactive astrocytes in the vestibular compensation process remains to be determined.